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Visual imagery deficits in posterior cortical atrophy
Abstract
Visual imagery has a close overlapping relationship with visual perception. Posterior cortical atrophy (PCA) is a neurodegenerative syndrome marked by early impairments in visuospatial processing and visual object recognition. We asked whether PCA would therefore also be marked by deficits in visual imagery, tested using objective forced-choice questionnaires, and whether imagery deficits would be selective for certain properties. We recruited four patients with PCA and a patient with integrative visual agnosia due to bilateral occipitotemporal strokes for comparison. We administered a test battery probing imagery for object shape, size, colour lightness, hue, upper-case letters, lower-case letters, word shape, letter construction, and faces. All subjects showed significant impairments in visual imagery, with imagery for lower-case letters most likely to be spared. We conclude that PCA subjects can show severe deficits in visual imagery. Further work is needed to establish how frequently this occurs and how early it can be found.
This study presents a neuropsychological evaluation of a unique case of prosopagnosia (patient EP) with atypical lesion patterns, characterized by intact face-selective nodes but significant damage to the Vertical Occipital Fasciculus (VOF). Given the presumed interruption of ventral-parietal connectivity, we focused on assessing the potential presence of simultanagnosia and its potential relationship to his face recognition deficits. Our neuropsychological battery included tests of global and local processing, scene perception, and face recognition. Results revealed intact global processing abilities and no evidence of simultanagnosia, despite the patient's prosopagnosia. These findings suggest that EP's face recognition impairment is likely attributable to disrupted connectivity within the face processing network rather than a general deficit in global/holistic processing. This case highlights the importance of comprehensive neuropsychological assessments in atypical presentations of prosopagnosia and contributes to our understanding of the complex relationship between white matter integrity and face recognition abilities.
The year 2021 marks the 130th anniversary of the untimely death of Heinrich Lissauer (1861-1891). In his thirty years of life, Lissauer managed to put together an impressive number of contributions to neurology and neuroanatomy. Most influential is his famous distinction between apperceptive and associative forms of visual agnosia. It is perhaps less well-known that in the same article, Lissauer outlined a model of possible dissociations between visual perception and visual mental imagery. Drawing on Hermann Munk’s animal experiments, Lissauer proposed that complete destruction of occipital visual cortex would provoke both perception and imagery deficits, whereas its deafferentation resulting from subcortical white matter damage would only affect visual perception, and leave visual memories unimpaired. This proposal resonates with the present debate on the neural bases of visual mental imagery.
Objectives:
Posterior Cortical Atrophy (PCA) is an atypical presentation of Alzheimer disease (AD) characterized by atrophy of posterior brain regions. This pattern of atrophy is usually evaluated with Koedam visual rating scale, a score developed to enable visual assessment of parietal atrophy on magnetic resonance imaging (MRI). However, Koedam scale is complex to assess and its utility in the differential diagnosis between PCA and typical AD has not been demonstrated yet. The aim of this study is therefore to spot a simple and reliable MRI element able to differentiate between PCA and typical AD using visual rating scales.
Methods:
15 patients who presented with progressive complex visual disorders and predominant occipitoparietal hypometabolism on PET-FDG were selected from our centre and compared with 30 typical AD patients and 15 healthy subjects. We used previously validated visual rating scales including Koedam scale, which we divided into three major components: posterior cingulate, precuneus and parieto-occipital. Subsequently we validated the results using the automated software Brainvisa Morphologist and Voxel Based Morphometry (VBM).
Results:
Patients with PCA, compared to typical AD, showed higher widening of the parieto-occipital sulcus, assessed both with visual rating scales and Brainvisa. In the corresponding areas, the VBM analysis showed an inverse correlation between the results obtained from the visual evaluation scales with the volume of the grey matter and a direct correlation between the same results with the cerebrospinal fluid volume.
Conclusions:
A visually based rating scale for parieto-occipital sulcus can distinguish Posterior Cortical Atrophy from typical Alzheimer disease.
While the loss of mental imagery following brain lesions was first described more than a century ago, the key cerebral areas involved remain elusive. Here we report neuropsychological data from an architect (PL518) who lost his ability for visual imagery following a bilateral posterior cerebral artery (PCA) stroke. We compare his profile to three other patients with bilateral PCA stroke and another architect with a large PCA lesion confined to the right hemisphere. We also compare structural images of their lesions, aiming to delineate cerebral areas selectively lesioned in acquired aphantasia. When comparing the neuropsychological profile and structural magnetic resonance imaging (MRI) for the aphantasic architect PL518 to patients with either a comparable background (an architect) or bilateral PCA lesions, we find: (1) there is a large overlap of cognitive deficits between patients, with the very notable exception of aphantasia which only occurs in PL518, and (2) there is large overlap of the patients’ lesions. The only areas of selective lesion in PL518 is a small patch in the left fusiform gyrus as well as part of the right lingual gyrus. We suggest that these areas, and perhaps in particular the region in the left fusiform gyrus, play an important role in the cerebral network involved in visual imagery.
Posterior cortical atrophy is a clinico-radiological syndrome characterized by progressive decline in visual processing and atrophy of posterior brain regions. With the majority of cases attributable to Alzheimer’s disease and recent evidence for genetic risk factors specifically related to posterior cortical atrophy, the syndrome can provide important insights into selective vulnerability and phenotypic diversity. The present study describes the first major longitudinal investigation of posterior cortical atrophy disease progression. Three hundred and sixty-one individuals (117 posterior cortical atrophy, 106 typical Alzheimer’s disease, 138 controls) fulfilling consensus criteria for posterior cortical atrophy-pure and typical Alzheimer’s disease were recruited from three centres in the UK, Spain and USA. Participants underwent up to six annual assessments involving MRI scans and neuropsychological testing. We constructed longitudinal trajectories of regional brain volumes within posterior cortical atrophy and typical Alzheimer’s disease using differential equation models. We compared and contrasted the order in which regional brain volumes become abnormal within posterior cortical atrophy and typical Alzheimer’s disease using event-based models. We also examined trajectories of cognitive decline and the order in which different cognitive tests show abnormality using the same models. Temporally aligned trajectories for eight regions of interest revealed distinct (P < 0.002) patterns of progression in posterior cortical atrophy and typical Alzheimer’s disease. Patients with posterior cortical atrophy showed early occipital and parietal atrophy, with subsequent higher rates of temporal atrophy and ventricular expansion leading to tissue loss of comparable extent later. Hippocampal, entorhinal and frontal regions underwent a lower rate of change and never approached the extent of posterior cortical involvement. Patients with typical Alzheimer’s disease showed early hippocampal atrophy, with subsequent higher rates of temporal atrophy and ventricular expansion. Cognitive models showed tests sensitive to visuospatial dysfunction declined earlier in posterior cortical atrophy than typical Alzheimer’s disease whilst tests sensitive to working memory impairment declined earlier in typical Alzheimer’s disease than posterior cortical atrophy. These findings indicate that posterior cortical atrophy and typical Alzheimer’s disease have distinct sites of onset and different profiles of spatial and temporal progression. The ordering of disease events both motivates investigation of biological factors underpinning phenotypic heterogeneity, and informs the selection of measures for clinical trials in posterior cortical atrophy.
This study aimed to investigate the association between HLA genotypes and antiepileptic drug-induced cutaneous adverse reactions (AEDs-cADRs) among patients with epilepsy in Ningxia Hui Autonomous Region of Northwest China. Fifteen patients with AEDs-cADRs and 30 matched AEDs tolerant controls from anested case-control study were tested the HLA-A, HLA-B, and HLA-DRB1 genotype using the polymerase chain reaction sequence-based typing (PCR-SBT). Significant difference was not observed between AEDs-cADRs and AEDs tolerant groups in terms of HLA-A, HLA-B, and HLA-DRB1 genotype frequencies. Future studies using larger cohorts are needed to verify this observation.
Introduction:
A classification framework for posterior cortical atrophy (PCA) is proposed to improve the uniformity of definition of the syndrome in a variety of research settings.
Methods:
Consensus statements about PCA were developed through a detailed literature review, the formation of an international multidisciplinary working party which convened on four occasions, and a Web-based quantitative survey regarding symptom frequency and the conceptualization of PCA.
Results:
A three-level classification framework for PCA is described comprising both syndrome- and disease-level descriptions. Classification level 1 (PCA) defines the core clinical, cognitive, and neuroimaging features and exclusion criteria of the clinico-radiological syndrome. Classification level 2 (PCA-pure, PCA-plus) establishes whether, in addition to the core PCA syndrome, the core features of any other neurodegenerative syndromes are present. Classification level 3 (PCA attributable to AD [PCA-AD], Lewy body disease [PCA-LBD], corticobasal degeneration [PCA-CBD], prion disease [PCA-prion]) provides a more formal determination of the underlying cause of the PCA syndrome, based on available pathophysiological biomarker evidence. The issue of additional syndrome-level descriptors is discussed in relation to the challenges of defining stages of syndrome severity and characterizing phenotypic heterogeneity within the PCA spectrum.
Discussion:
There was strong agreement regarding the definition of the core clinico-radiological syndrome, meaning that the current consensus statement should be regarded as a refinement, development, and extension of previous single-center PCA criteria rather than any wholesale alteration or redescription of the syndrome. The framework and terminology may facilitate the interpretation of research data across studies, be applicable across a broad range of research scenarios (e.g., behavioral interventions, pharmacological trials), and provide a foundation for future collaborative work.
This study investigated the cognitive profile and the cerebral perfusion pattern in a highly educated 70 year old gentleman with posterior cortical atrophy (PCA). Visuo-perceptual abilities, spatial memory, spatial representation and navigation, visuo-spatial mental imagery, semantic and episodic-autobiographical memory were assessed. Regional cerebral blood flow (rCBF) was imaged with SPECT. Cognitive testing showed visual-perceptual impairment, apperceptive visual and landmark agnosia, topographical disorientation with way-finding deficits, impaired map learning and poor mental image generation. Semantic memory was normal, while episodic-autobiographical memory was impaired. Reduced rCBF was found mainly in the right hemisphere, in the precentral gyrus, posterior cingulate and middle temporal gyri, cuneus and precuneus, in the left superior temporal and lingual gyri and in the parahippocampus bilaterally. Hypoperfusion in occipito-parietal regions was associated with visuo-spatial deficits, whereas deficits in visuo-spatial mental imagery might reflect dysfunction related to hypoperfusion in the parahippocampus and precuneus, structures which are responsible for spatial and imagery processing. Dissociating performance between preserved semantic memory and poor episodic-autobiographical recall is consistent with a pattern of normal perfusion in frontal and anterior temporal regions but abnormal rCBF in the parahippocampi. The present findings indicate that PCA involves visuo-spatial imagery deficits and provide further validation to current neuro-cognitive models of spatial representation and topographical disorientation.
Naming or word-finding tasks are a mainstay of the typical neuropsychological evaluation, particularly with older adults. However, many older adults have significant visual impairment and there are currently no such word-finding tasks developed for use with older visually impaired populations. This study presents a verbal, non-visual measure of word-finding for use in the evaluation of older adults with possible dysnomia. Stimuli were chosen based on their frequency of usage in everyday spoken language. A 60-item scale was created and given to 131 older Veterans. Rasch analyses were conducted and differential item functioning assessed to eliminate poorly-performing items. The final 55-item scale had a coefficient alpha of 0.84 and correlated with the Neuropsychological Assessment Battery Naming test, r=0.84, p<.01, Delis-Kaplan Executive Function System (D-KEFS) Category Fluency, r=0.45, p<.01, and the D-KEFS Letter Fluency, r=0.40, p<.01. ROC analyses found the measure to have sensitivity of 79% and specificity of 85% for detecting dysnomia. Patients with dysnomia performed worse on the measure than patients with intact word-finding, t(84)=8.2, p<.001. Patients with no cognitive impairment performed significantly better than patients with mild cognitive impairment, who performed significantly better than patients with dementia. This new measure shows promise in the neuropsychological evaluation of word-finding ability in older adults with or without visual impairment. Future directions include the development of a shorter version and the generation of additional normative data. (JINS, 2015, 21, 1-10).
Normative data stratified by three levels of age (16–59, 60–79, and 80–95 years) and three levels of education (0–8, 9–12, and 13–21 years) are presented for phonemic verbal fluency (FAS) and categorical verbal fluency (Animal Naming). The normative sample, aged 16 to 95 years, consisted of 1,300 cognitively intact individuals who resided in the community. Years of education ranged from 0 to 21. The total number of words in 1 minute for each of the letters F, A, and S was correlated r = .52 with the number of animal names generated in 1 minute. Regression analyses showed that FAS was more sensitive to the effects of education (18.6% of the variance) than age (11.0% of the variance). The opposite relationship occurred for Animal Naming, where age accounted for 23.4% of the variance and education accounted only for 13.6%. Gender accounted for less than 1% of variance for FAS and Animal Naming. The clinical utility of these norms is discussed.
A patient with associative visual agnosia secondary to a penetrating bitemporooccipital lesion remained able to draw complex objects from memory but could not subsequently recognize his sketches. His retained ability to copy and draw briefly exposed objects indicates that this is not a problem of visual perception. On tasks of categorization, mental imagery, drawing, and object decision, he demonstrates many instances of preserved visual semantic memories and imagery despite a sense of unfamiliarity with the visual stimuli. We infer a preserved ability to derive internal visual images from semantic memory. Cues may help him visualize the named object, which then serves as a model for comparison with the actual stimulus. However, his adequate visual perception and mental visual imagery, even when assisted by cues, are still insufficient to correct fully his difficulty in recognizing objects. Unique to his case is an inability to match the representation of stimulus objects with his intact internal image of the same object. Deficient lateral inhibition between neural representations of similar objects may be responsible.
We argue that the debate over whether mental images are visual or spatial representations is based on the false premise that they must be one or the other. In support of the hypothesis that mental imagery has distinct visual and spatial components of representation, we (1) point out a correspondence between the notions of visual appearance and spatial location representations in visual neurophysiology, on the one hand, and the notions of visual and spatial representations as used in the debate about mental imagery, on the other; and (2) present the performance of a brain-damaged patient with impaired visual appearance representations on a variety of tasks used by cognitive psychologists on one side or other of the visual vs spatial imagery debate. The patient is severely impaired on tasks previously used to argue for the visual nature of imagery, but performs normally on tasks previously used to argue for the spatial nature of imagery. This implies that the two groups of tasks tap distinct types of representation, which are neurologically dissociable and hence comprise functionally independent subsystems of imagery representation.
The paper reports the investigation of a 26-year-old man affected by cortical blindness for over 4 years. The patient showed a remarkable preservation of intelligence, language skills and a very mild memory disorder. He was, however, unable to perform any tasks requiring the use of information related to the visual appearance of places, symbols, objects and animals. In contrast, the performance on tasks exploring his knowledge of functional aspects of objects, animals and vegetables was unimpaired. This neuropsychological profile could be explained by an inability to derive internal visual images from long-term memory, which would drastically reduce the ability to retrieve visual semantic memories. Assessments of cerebral metabolism with [18F]FDG and PET revealed a calcarine and associative occipital hypometabolism, extending to the inferior and mesial temporal cortex.
The Rey–Osterrieth Complex Figure Test (ROCF), which was developed by Rey in 1941 and standardized by Osterrieth in 1944, is a widely used neuropsychological test for the evaluation of visuospatial constructional ability and visual memory. Recently, the ROCF has been a useful tool for measuring executive function that is mediated by the prefrontal lobe. The ROCF consists of three test conditions: Copy, Immediate Recall and Delayed Recall. At the first step, subjects are given the ROCF stimulus card, and then asked to draw the same figure. Subsequently, they are instructed to draw what they remembered. Then, after a delay of 30 min, they are required to draw the same figure once again. The anticipated results vary according to the scoring system used, but commonly include scores related to location, accuracy and organization. Each condition of the ROCF takes 10 min to complete and the overall time of completion is about 30 min.
Using diffusion tensor magnetic resonance imaging tractography, ventral (inferior longitudinal fasciculus) and fronto-occipital (inferior fronto-occipital fasciculus) and dorsal (fronto-parietal superior longitudinal fasciculus) visual pathways were assessed in 7 patients with posterior cortical atrophy (PCA), showing either predominantly ventral or additional dorsal cognitive deficits. Corpus callosum and corticospinal tracts were also studied. Gray and white matter atrophy was assessed using voxel-based morphometry. In all PCA patients, abnormal diffusivity indexes were found in bilateral inferior longitudinal fasciculus and inferior fronto-occipital fasciculus, with a left-side predominance. Patients also had mild microstructural damage to the corpus callosum. The 2 patients with more dorsal symptoms also showed right fronto-parietal superior longitudinal fasciculus abnormalities. Corticospinal tracts were normal, bilaterally. When studied separately, patients with ventral clinical impairment showed a pattern of atrophy mainly located in the ventral occipitotemporal regions, bilaterally; patients with both ventral and dorsal clinical deficits showed additional atrophy of the bilateral inferior parietal lobe. Magnetic resonance imaging patterns of abnormalities mirror closely the clinical phenotypes and could provide reliable ante mortem markers of tissue damage in PCA.
This study was designed to investigate the impact of semantic deficits on the recognition of words and objects as real/familiar. Two-alternative forced-choice tasks of lexical decision and object decision were each administered to a case series of patients with semantic dementia. In both tasks, the critical manipulation was whether the real word or object was more or less "natural" (i.e., typical of its domain) than the nonword or nonobject with which it was paired. For lexical decision, typicality of the words and nonwords was manipulated in terms of bigram and trigram frequencies of the letter strings. For object decision, high typicality in real and chimeric objects consisted in having only or mainly visual features that are standard for objects in that category. This manipulation of relative typicality of real and made-up stimuli exerted a dramatic influence on the patients' success in both lexical and object decision. The patients' strong tendency towards "natural selection" was further modulated by both the frequency/familiarity of the real words/objects and the degree of semantic degradation of the individual patients. This outcome is in line with the authors' model of semantic knowledge and the impact of its degradation on a wide range of cognitive behaviour.
It is increasingly common for group studies in neuropsychology to report effect sizes. In contrast this is rarely done in single-case studies (at least in those studies that employ a case-controls design). The present paper sets out the advantages of reporting effect sizes, derives suitable effect size indexes for use in single-case studies, and develops methods of supplementing point estimates of effect sizes with interval estimates. Computer programs that implement existing classical and Bayesian inferential methods for the single case (as developed by Crawford, Garthwaite, Howell, and colleagues) are upgraded to provide these point and interval estimates. The upgraded programs can be downloaded from www.abdn.ac.uk/~psy086/dept/Single_Case_Effect_Sizes.htm.
Acquired prosopagnosia varies in both behavioural manifestations and the location and extent of underlying lesions. We studied 10 patients with adult-onset lesions on a battery of face-processing tests. Using signal detection methods, we found that discriminative power for the familiarity of famous faces was most reduced by bilateral occipitotemporal lesions that involved the fusiform gyri, and better preserved with unilateral right-sided lesions. Tests of perception of facial structural configuration showed severe deficits with lesions that included the right fusiform gyrus, whether unilateral or bilateral. This deficit was most consistent for eye configuration, with some patients performing normally for mouth configuration. Patients with anterior temporal lesions had better configuration perception, though at least one patient showed a more subtle failure to integrate configural data from different facial regions. Facial imagery, an index of facial memories, was severely impaired by bilateral lesions that included the right anterior temporal lobe and marginally impaired by fusiform lesions alone; unilateral right fusiform lesions tended to spare imagery for facial features. These findings suggest that (I) prosopagnosia is more severe with bilateral than unilateral lesions, indicating a minor contribution of the left hemisphere to face recognition, (2) perception of facial configuration critically involves the right fusiform gyrus and (3) access to facial memories is most disrupted by bilateral lesions that also include the right anterior temporal lobe. This supports assertions that more apperceptive variants of prosopagnosia are linked to fusiform damage, whereas more associative variants are linked to anterior temporal damage. Next, we found that behavioural indices of covert recognition correlated with measures of overt familiarity, consistent with theories that covert behaviour emerges from the output of damaged neural networks, rather than alternative pathways. Finally, to probe the face specificity of the prosopagnosic defect, we tested recognition of fruits and vegetables: While face specificity was not found in most of our patients, the data of one patient suggested that this may be possible with more focal lesions of the right fusiform gyrus.
Visual imagery is the creation of mental representations that share many features with veridical visual percepts. Studies of normal and brain-damaged people reinforce the view that visual imagery and visual perception are mediated by a common neural substrate and activate the same representations. Thus, brain-damaged patients with intact vision who have an impairment in perception should have impaired visual imagery. Here we present evidence to the contrary from a patient with severely impaired object recognition (visual object agnosia) but with normal mental imagery. He draws objects in considerable detail from memory and uses information derived from mental images in a variety of tasks. In contrast, he cannot identify visually presented objects, even those he has drawn himself. He has normal visual acuity and intact perception of equally complex material in other domains. We conclude that rich internal representations can be activated to support visual imagery even when they cannot support visually mediated perception of objects.
The intuition that imagery is similar to perception has led many psychologists to assume that imaging an object consists of activating some of the same representational structures that are activated during the perception of that object. This assumption was tested by measuring the effects of visual imagery on concurrent visual perception. The experimental task consisted of a two-interval forced-choice detection task (no stimulus identification required) during which the subject imaged a particular stimulus. In Experiment 1, a matching image led to better detection than a nonmatching image. Interactions between imagery and perception imply a common locus of activity, and the content-specific interactions obtained here imply that the common locus consists of representational structures. In Experiment 2, a matching image facilitated perception only when the image and the stimulus were in the same position. This was taken to imply that the shared representational structures occur at an analog level of perceptual representation.
We describe a patient with a deficit in imagery ability, following a left posterior cerebral artery infarction and possible anoxic episode. This deficit was inferred from the patient's performance on several tasks, including one in which normal adults are known to rely on imagery and two that tested imagery nonverbally, allowing us to examine the possibility of a language-imagery disconnection. In addition, we queried the patient on some cognitive capacities related to visual imagery: dreaming, geographical knowledge, and introspection regarding visual and auditory imagery. Hypotheses concerning the critical lesion site and underlying cognitive mechanism of image generation deficits are discussed in relation to this and other recent cases of impaired imagery ability with intact recognition ability, and the relevance of this deficit to the "imagery debate" is discussed.
We studied two patients with impaired visual perception and imagery caused by bilateral posterior cerebral lesions. The first had prosopagnosia and achromatopsia, and the imagery disorder involved the description of objects from memory, especially faces and animals, and colors of objects. The second had visual disorientation; the imagery problem involved the description of spatial relations from memory. Impairments of visual imagery, like disorders of visual perception, can be dissociated. Object and color imagery may be dissociated from imagery for spatial relations. A given imagery deficit tends to be associated with the corresponding type of perceptual deficit.
Detection of a visual target can be facilitated by flanking visual masks. A similar enhancement in detection thresholds was
obtained when observers imagined the previously perceived masks. Imagery-induced facilitation was detected for as long as
5 minutes after observation of the masks by the targeted eye. These results indicated the existence of a low-level (monocular)
memory that stores the sensory trace for several minutes and enables reactivation of early representations by higher processes.
This memory, with its iconic nature, may subserve the interface between mental images and percepts.
Although it is now well accepted that visual mental imagery and visual perception share common underlying mechanisms, there are several reports in which they are dissociated. Evidence for the separability of these processes is provided by a patient, C.K., who has a profound visual object recognition deficit attributable to an impairment in grouping or segmenting visual images. Despite this perceptual deficit, C.K. was able to draw objects in considerable detail from memory, and his knowledge of the visual appearance of objects was preserved on a variety of mental imagery tasks. Together with previous cases, these findings confirm the double dissociation between object recognition and perception. Interestingly, C.K. could also recognize newly constructed objects in his internal imagery. To accommodate these results, we propose a model in which imagery and perception are strongly associated but are also functionally specialized.
Subjects with complete ocular blindness in both eyes provide a unique opportunity to study the long-term durability of visual semantic memory. In this cross-sectional study we recruited eleven subjects who had acquired blindness for between 1 and 36 years. For comparison, we studied four subjects with congenital blindness and seventeen age- and sex-matched sighted control subjects. We administered ten forced-choice questionnaires that probed one auditory category and four visual categories, namely object shape and size; object hue and lightness; word and letter shape; and the shape and features of famous faces. Subjects with congenital blindness performed worse than controls on all visual categories, but nevertheless performed better than chance on object structure or colour, suggesting that the answers to some questions about visual properties can be derived from haptic or non-visual semantic information. Subjects with acquired blindness performed similarly to controls on all categories except for facial memory, particularly for facial features. We conclude that there is a substantial “permastore” of visual semantic memory but that facial memories are less durable, perhaps indicating that they are either less over-learned or more dependent on visual representations than other forms of visual object information.
Background
Posterior cortical atrophy (PCA) is a neurocognitive disorder characterized by difficulty localizing in space. Recognizing PCA is important because it is usually missed early in its course and may result from a number of neurological disorders other than Alzheimer's disease (AD).
Objective
This study aimed to clarify whether impaired visual search tasks of spatial localization distinguished patients with PCA from those with other more typical dementias as well as from healthy control (HC) subjects.
Methods
Twelve patients meeting neuroimaging-supported Consensus Criteria for PCA, 12 comparably advanced patients with amnestic-predominant typical AD (tAD), and 24 HC participants were compared on tests of untimed and timed visual search, spatial neglect, mental rotation, environmental orientation, visuospatial construction, and face recognition.
Results
Only abnormalities in untimed and timed visual search and environmental orientation distinguished the PCA patients from both the tAD group and the HC group without also distinguishing the tAD patients from HC's. The PCA patients also had a tendency to greater difficulty scanning left hemispace compared to HC's. Visuospatial constructions, although worse in PCA, and face recognition were impaired in both dementia groups.
Conclusions
These findings support the concept of PCA as a disorder of spatial processing and localization, indicating that visual search tasks are particularly sensitive and specific for detecting PCA and distinguishing it from more typical dementia syndromes.
In the absence of input from the external world, humans are still able to generate vivid mental images. This cognitive process, known as visual mental imagery, involves a network of prefrontal, parietal, inferotemporal, and occipital regions. Using multivariate pattern analysis (MVPA), previous studies were able to distinguish between the different orientations of imagined gratings, but not between more complex imagined stimuli, such as common objects, in early visual cortex (V1). Here asked whether letters, simple shapes, and objects can be decoded in early visual areas during visual mental imagery. In a delayed spatial judgment task, we asked participants to observe or imagine stimuli. To examine whether it is possible to discriminate between neural patterns during perception and visual mental imagery, we performed ROI-based and whole-brain searchlight-based MVPA. We were able to decode imagined stimuli in early visual (V1, V2), parietal (SPL, IPL, aIPS), inferotemporal (LOC) and prefrontal (PMd) areas. In a subset of these areas (i.e. V1, V2, LOC, SPL, IPL and aIPS), we also obtained significant cross-decoding across visual imagery and perception. Moreover, we observed a linear relationship between behavioral accuracy and the amplitude of the BOLD signal in parietal and inferotemporal cortices, but not in early visual cortex, in line with the view that these areas contribute to the ability to perform visual imagery. Together, our results suggest that in the absence of bottom-up visual inputs, patterns of functional activation in early visual cortex allow distinguishing between different imagined stimulus exemplars, most likely mediated by signals from parietal and inferotemporal areas.
Mental imagery can be advantageous, unnecessary and even clinically disruptive. With methodological constraints now overcome, research has shown that visual imagery involves a network of brain areas from the frontal cortex to sensory areas, overlapping with the default mode network, and can function much like a weak version of afferent perception. Imagery vividness and strength range from completely absent (aphantasia) to photo-like (hyperphantasia). Both the anatomy and function of the primary visual cortex are related to visual imagery. The use of imagery as a tool has been linked to many compound cognitive processes and imagery plays both symptomatic and mechanistic roles in neurological and mental disorders and treatments. Mental imagery plays a role in a variety of cognitive processes such as memory recall. In this review, Joel Pearson discusses recent insights into the neural mechanisms that underlie visual imagery, how imagery can be objectively and reliably measured, and how it affects general cognition.
For decades, the extent to which visual imagery relies on the same neural mechanisms as visual perception has been a topic of debate. Here, we review recent neuroimaging studies comparing these two forms of visual experience. Their results suggest that there is a large overlap in neural processing during perception and imagery: neural representations of imagined and perceived stimuli are similar in the visual, parietal, and frontal cortex. Furthermore, perception and imagery seem to rely on similar top-down connectivity. The most prominent difference is the absence of bottom-up processing during imagery. These findings fit well with the idea that imagery and perception rely on similar emulation or prediction processes.
Posterior Cortical Atrophy (PCA) is a rare neurodegenerative syndrome characterised by profound visuoperceptual processing disturbances, attributable to focal parieto-occipital cortical atrophy. Despite relative sparing of the medial temporal lobes, converging evidence reveals significant autobiographical memory impairments in this syndrome, underscoring the crucial role of visual imagery for episodic memory processes. The contribution of visual imagery to complex constructive endeavours, however, remains unclear. Here, we investigated the capacity for atemporal scene construction in 5 well-characterised cases of PCA and contrasted their performance with 10 typical amnestic Alzheimer’s Disease (AD) and 10 healthy older Control participants. Behavioural data were analysed using case-Control statistics comparing each PCA patient’s scene construction scores to the mean scores of AD and Control groups. In keeping with their clinical phenotype, PCA patients demonstrated significant visuoperceptual and episodic memory impairments on standard neuropsychological tasks. Scene construction performance was grossly impaired in PCA, at a level comparable to that observed in the AD group, manifesting in impoverished and spatially fragmented scenes. Structural neuroimaging confirmed prominent grey matter intensity decrease predominantly in posterior cortical regions in PCA, in the absence of frank hippocampal atrophy. Using an a priori motivated region-of-interest approach across all participants, scene construction performance was found to correlate with grey matter intensity in the left angular gyrus, right precuneus, and right hippocampus. This study is the first to reveal compromised scene construction capacity in PCA, extending our understanding of the cognitive profile of this rare syndrome and pointing towards the fundamental contribution of visual imagery to atemporal forms of imagination.
Posterior cortical atrophy is a neurodegenerative syndrome characterised by progressive disruption of visual and perceptual processing, associated with atrophy in the parieto-occipital cortex. Current diagnostic criteria describe relative sparing of episodic memory function, but recent findings suggest that anterograde memory is often impaired. Whether these deficits extend to remote memory has not been addressed. A large body of evidence suggests that the recollection of an autobiographical event from the remote past coincides with the successful retrieval of visual images. We hypothesised that the profound visual processing deficits in posterior cortical atrophy would result in impaired autobiographical memory retrieval. Fourteen posterior cortical atrophy patients, eighteen typical Alzheimer's disease patients and twenty-eight healthy controls completed the Autobiographical Interview. Autobiographical memory in posterior cortical atrophy was characterised by a striking loss of internal, episodic detail relative to controls and to same extent as typical Alzheimer's disease patients, in conjunction with an increase in external details tangential to the memory described. The memory narratives of posterior cortical atrophy patients showed a specific reduction in spatiotemporal and perceptual detail. Voxel-based morphometry analysis revealed atrophy of the parieto-occipital cortices in posterior cortical atrophy but relatively spared hippocampi bilaterally, compared with characteristic atrophy of the medial temporal lobes in typical Alzheimer's disease. Analysis of brain regions showing posterior cortical atrophy-specific atrophy revealed a correlation between perceptual details in autobiographical memory and grey matter density in the right precuneus. This study demonstrates remote memory impairment in posterior cortical atrophy despite relatively preserved medial temporal lobe structures. The results demonstrate, for the first time, profound autobiographical memory impairment in PCA and suggest that this is driven by the well-recognised deficits in higher-order visual processing. The findings are discussed in the context of posterior parietal contributions to imagery and memory, and the clinical implications of autobiographical memory impairment for diagnostic and management protocols in posterior cortical atrophy.
The Addenbrooke’s Cognitive Examination (ACE) was originally developed as a theoretically motivated extension of the Mini-Mental State Examination (MMSE) which attempted to address the neuropsychological omissions and improve the screening performance of the latter. Though taking longer to administer than the MMSE, and therefore best suited to specialist settings, ACE and its subsequent iterations, ACE-R and ACE-III, have proved easy to use, acceptable to patients, and have shown excellent diagnostic utility in identifying dementia and cognitive impairment in a variety of clinical situations (Alzheimer’s disease, frontotemporal lobar degenerations, Parkinsonian syndromes, stroke and vascular dementia, brain injury). The most recent development, the Mini-Addenbrooke’s Cognitive Examination (M-ACE), takes no more time to administer than the MMSE but, like the longer versions, is superior to MMSE in diagnostic utility. The utility of ACE/ACE-R has prompted translation into various languages, and this trend is anticipated to continue for ACE-III and M-ACE.
Describes the construction of a graded difficulty test of concrete and abstract word synonym comprehension. The standardization sample consisted of 184 volunteers (aged 16–77 yrs) representing a cross-section of the population. Percentile scores and scaled scores are presented for each section of the test. The test was validated in an experimental group of 65 with unilateral cerebral lesions in the left or right hemispheres. The greatest impairments were observed in Ss with left temporal lobe lesions. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Adaptive behavior guided by unconscious visual cues occurs in patients with various kinds of brain damage as well as in normal observers, all of whom can process visual information of which they are fully unaware [1] [2] [3] [4] [5] [6] [7] [8]. Little is known on the possibility that unconscious vision is influenced by visual cues that have access to consciousness [9]. Here we report a 'blind' letter discrimination induced through a semantic interaction with conscious color processing in a patient who is agnosic for visual shapes, but has normal color vision and visual imagery. In seeing the initial letters of color names printed in different colors, it is normally easier to name the print color when it is congruent with the initial letter of the color name than when it is not [10]. The patient could discriminate the initial letters of the words 'red' and 'green' printed in the corresponding colors significantly above chance but without any conscious accompaniment, whereas he performed at chance with the reverse color-letter mapping as well as in standard tests of letter reading. We suggest that the consciously perceived colors activated a representation of the corresponding word names and their component letters, which in turn brought out a partially successful, unconscious processing of visual inputs corresponding to the activated letter representations.
It has been reported that congenital prosopagnosics may have a general imagery deficit or an imagery deficit specific to faces. However, much of this evidence is based on self-report questionnaires, rather than experimentally based testing (Grüter et al., 2007, 2009). This study tested face and non-face based imagery in a case series of congenital prosopagnosics, utilising both questionnaire based and forced choice accuracy measures. Our findings indicate that all the prosopagnosics showed impaired face based imagery, which contrasted with normal performance on imagery of objects and colours - a pattern that is consistent with reports of acquired prosopagnosia (Barton, 2008; Michelon and Biederman, 2003). Given all our experimentally based testing indicated face imagery impairments, despite no such problems being seen on self-report questionnaires, we would argue that testing based only on the latter must be interpreted with some caution. Overall, we would advocate that our findings demonstrate a category specific visual imagery impairment in congenital prosopagnosia, such that general imagery skill can be intact in such cases.
STANDARD texts on differential psychology often discuss briefly the existence of sex differences in the ability to perform various cognitive tasks1-3. A rough generalisation is that females perform better than males on verbal tasks (for example, verbal fluency, articulation, spelling), whilst males are superior on visuospatial tasks (for example, maze learning or form-board tasks), although exceptions are plentiful. In view of the emphasis in contemporary cognitive psychology on the pervasiveness of verbal coding in a variety of cognitive tasks, and also current interest in such visuospatial abilities as visual imagery or mental rotation, it seems surprising that no attention has been paid to the possible existence of sex differences.
A case is reported of an associative visual agnosic patient who could not draw from memory objects he could recognize, even though he could copy drawings flawlessly. His ability to generate mental visual images was found to be spared, as was his ability to operate upon mental images. These data suggest that the patient could generate mental images but could not draw from memory because he did not have access to stored knowledge about pictorial attributes of objects. A similar functional impairment can be found in some other visual agnosic patients and in patients affected by optic aphasia. The present case allows a discussion of relationships among drawing from memory, imagery, and copying procedures.
Experiments were designed to examine the imagery abilities of an agnosic patient, M.S., who has consistently shown more severe deficits in recognizing visually, and in retrieving knowledge of living as compared with non-living items. Judgements of visual similarity were required for named objects and for object-pictures, as well as for the factual properties of these stimuli. The same disproportionate difficulty in processing living ('natural') objects was found in these tasks as well as in forced-choice recognition. In contrast, no deficit was found on analogous tasks concerned with word-shape similarities. These findings have a bearing on concepts of semantic memory.
Two subjects affected by pure alexia and showing no central dyschromatopsia or generalized aphasia, performed poorly on traditional tasks with visually-presented colour stimuli and on tasks with objects presented verbally. Three experiments were conducted to evaluate the possible role of mental colour imagery in recalling the colours of objects from memory. It was concluded that Case I, with left occipital lobe softening, had preserved imagery systems, but failed to recode the colours of mentally generated colour images, just as he failed to name visually presented colours, suggesting a language-imagery disconnection. In contrast, Case II, with a bilateral occipital lesion, had sustained damage to her long-term visual memories for colours as chromatic attributes of objects. This content-specific imagery deficit was concomitant with colour agnosia. The present findings are discussed in terms of current cognitive theories on imagery deficits.
The lateralization of visual mental imagery was investigated by presenting each hemisphere of a commissurotomy patient with a letter classification task known to require imagery and with a pair of control tasks designed to require all of the same processes as the imagery task except for the imagery processing itself. Whereas both hemispheres performed well on the control tasks, only the left hemisphere performed the imagery task.
The neurological literature contains numerous reports of loss of mental imagery following brain damage. This paper represents an attempt to interpret the patterns of deficits and preserved abilities in these reports in terms of a componential information-processing model of imagery. The principal result was a consistent pattern of deficit in a subset of patients, which could be attributed to a loss of the image generation component of imagery; examination of the lesion sites in this subset of patients implicated a region in the posterior left hemispheres as critical for the image generation process. The analysis also provided evidence that the long-term visual memories used in imagery are also used in recognition, and that dreaming and waking visual imagery share some underlying processes.RésuméOn trouve dans la litte´rature sur la neurologie de nombreux rapports sur la perte de l'imagerie mentalea`la suite d'atteintes ce´re´brales. Cet article pre´sente une interpre´tation des sche´mas de de´ficits et de conservations fonde´sur un mode`le componentiel du traitement de l'information. On montre qu'il existe un sche´ma de de´ficit cohe´rent pour deu sous-groupes de patients auxquels on peut attribuer une perte du composant de ge´ne´ration d'images. L'examen des sites de la lesion chez ces sujets circonscrit une re´gion de l'he´misphere poste´rieur gauche qui serait critique pour les processus de ge´ne´ration d'images. L'analyse montree´galement que les souvenirs visuelsa´long terme utilise´s dans l'imagerie sont aussi utilise´s pour la reconnaissance et que l'imagerie visuelle de l'e´veil partage avec celle du reve un certain nombre de processus sous-jacents.
A man with an infarction of his inferior temporal and occipital association cortex bilaterally, which spared primary visual cortex, had impaired visual recognition of objects, faces, colors, words, and gestures. Analysis of visual function indicated that the recognition failures resulted from an agnosia, rather than elemental visual impairment. Whereas his impairment of gesture recognition appeared to be related to an associative agnosia, his inability to recognize objects was related to an apperceptive agnosia. There may be four subtypes of apperceptive agnosia: one where the internal object representations or structural descriptions are impaired, another where an adequate percept cannot be derived, a third where the internal referent and percept are dissociated, and a fourth where both levels are impaired. Our patient demonstrated a failure to relate individual elements to the whole, a failure to integrate multiple elements, and a reliance on global perception. He had normal object imagery. These results suggest that, whereas internal representations were intact, he was unable to form adequate perceptual representations.
We describe a young woman, J.R., who sustained a very severe head injury in 1981 at the age of 17 years. She was assessed in 1982 and found to have visual agnosia. Since then J.R. has been assessed on several occasions over a period of ten years. Her agnosia for real objects has resolved and she has improved on the identification of other classes of stimuli. However, she still has some problems with the identification of line drawings, photographs and model animals. Her drawing from memory remains particularly poor and she has difficulty with visual imagery. We consider her residual deficits in the light of Farah's (1990) theoretical framework; this proposes that associative agnosia could be due to a disconnection syndrome, a loss of stored visual representations or to the loss of knowledge of how to perceive objects. J.R.'s residual impairments appear to be mainly due to a loss of access to visual representations in the absence of visual input.
A number of higher visual deficits accompanied by severe retrograde autobiographical memory loss following bilateral medial occipital infarctions are described in case M.H. Assessment of M.H.'s visual object agnosia and prospagnosia suggested that he was unable to integrate the elements of a percept to form a meaningful whole. This deficit may occur at the level the percept is encoded into the visual buffer and inspected. M.H. also describes a loss of visual memories, and it is hypothesized that this may similarly be a result of an inability to integrate the elements of the visual representation (e.g. of an object or face) following its generation from long-term visual memory store into the visual buffer. M.H.'s retrograde autobiographical memory loss is postulated to be a consequence of the severe impoverishment of episodic memories that must occur when events originally stored multimodally, must be recalled without any visual component.
We investigated the ability of a patient (D.F.) with profound visual form agnosia to perform a variety of tasks requiring visual imagery. Despite her inability to discriminate between objects and patterns of different shapes, sizes, and orientations, D.F. showed quite normal visual imagery involving these same 'visual' properties when the images were drawn from long-term memory. Thus, she was able both to scan mental images in search of particular features and to form new images by combining several known images. While there is growing evidence that perception and imagery share common neural substrates, the fact that D.F. shows intact visual imagery in the face of a massive perceptual deficit in form vision challenges recent suggestions that these two psychological processes share common input pathways in early vision. It is suggested that regions in the occipitotemporal pathway may be important for the generation of visual images while regions in the posterior parietal system might be involved in the manipulation of these images.